Effects of Abies holophylla Leaf Extract on Alcohol Metabolizing Enzyme Activity and Apoptosis in H₂O₂ and Ethanol-Induced HepG2 Cells

Abstract

This study investigated the protective effect of the Abies holophylla leaf extract on the alcohol metabolism enzyme activity and against H2O2 and ethanol-induced oxidative stress in HepG2 cells. The effect of Abies holophylla leaf extract on alcohol metabolism was determined by measuring the generation of reduced nicotinamide adenine dinucleotide (NADH) by alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH). ADH and ALDH activities of Abies holophylla leaf extract were increased in a dose-dependent manner (P<0.05), and were determined to be 155.53% and 130.89% at 1 mg/mL concentration, respectively. Exposure to the Abies holophylla leaf extract resulted in decreased levels of reactive oxygen species production in H2O2 and ethanol-induced HepG2 cells (P<0.05). Moreover, H2O2-induced HepG2 cells treated with the Abies holophylla leaf extract showed reduced expression of the pro-apoptotic protein Bax and increased expression of the anti-apoptotic protein Bcl-2 (P<0.05). Furthermore, Abies holophylla leaf extract treatment significantly decreased the protein expression of Bax in ethanol-induced HepG2 cells (P<0.05). However, the protein expression of Bcl-2 remained unaltered. Treatment with the Abies holophylla leaf extract also reduced the caspase-3 protein expression in H2O2 and ethanol-exposed HepG2 cells. In conclusion, our results indicate that the Abies holophylla leaf extract exerts a cytoprotective effect against H2O2 and ethanol-induced cell damage. We believe that the Abies holophylla leaf extract has the potential to be developed as a natural hepatoprotective agent.

Hangover-Relieving Effect of Ginseng Berry Kombucha Fermented by Saccharomyces cerevisiae and Gluconobacter oxydans in Ethanol-Treated Cells and Mice Model

“…Excessive production of ROS causes protein and DNA damage, cell death, tissue and organ damage, aging, and various diseases [ 2 ]. In addition, ethanol-induced oxidative stress in hepatocytes plays a key role in the development of alcoholic liver disease [ 3 ]. Therefore, the Nrf2 signaling pathway, which inhibits ROS generation and prevents lipid accumulation, is attracting attention for the development of drugs for alcoholic liver disease [ 4 ].…”